文献类型：期刊文献

中文题名：耐力训练对糖尿病GK大鼠有氧呼吸调节通路基因表达的影响

英文题名：Effects of endurance training on the gene expression of the aerobic respiration regulating path of diabetic GK rats

作者：邵月[1]

机构：[1]河南财经政法大学体育部

第一机构：河南财经政法大学体育部（系）

年份：2012

卷号：19

期号：2

起止页码：142-144

中文期刊名：体育学刊

外文期刊名：Journal of Physical Education

收录：CSTPCD;;国家哲学社会科学学术期刊数据库;北大核心:【北大核心2011】；CSSCI:【CSSCI2012_2013】；

基金：河南省科学技术厅基础与前言研究项目(112300410216);河南财经政法大学重大研究课题资金资助(2011-27)

语种：中文

中文关键词：运动生物化学;耐力训练;有氧呼吸;糖尿病;大鼠

外文关键词：sports biochemistry; endurance training; aerobic respiration; diabetes; rat

摘要：为探讨耐力训练对糖尿病大鼠骨骼肌有氧呼吸调节通路基因表达的影响,将12只大鼠随机分为2组:安静组(GKC,n=6只)、耐力训练组(GKE,n=6只)。GKE组跑台训练6周。末次训练后的24～48 h内切取腓肠肌,Real-time PCR检测p53、SCO2和COXII的mRNA转录,Western blot检测p53、SCO2和COXII的蛋白表达。结果发现:1)GKE组p53基因转录和蛋白表达水平与GKC组相比均显著降低;2)GKE组与GKC组相比SCO2基因转录和蛋白表达水平差异没有显著性;3)KE组COXII基因转录水平与GKC组相比差异没有显著性,但GKE组COXII蛋白表达水平非常显著低于GKC组。结果说明:耐力训练不能显著促进糖尿病大鼠线粒体有氧呼吸能力。COXII蛋白表达水平的显著下调似乎显示本实验耐力训练模型对其有氧呼吸轴有损害作用,但综合p53基因表达显著下调结果谨慎推测,这也许是受糖尿病病程影响,p53基因表达水平无法继续维持在正常稳态,其基因表达能力的下降极有可能是为了促进细胞的生存,也许是为了延缓GK大鼠病态细胞的凋亡或衰老进程。在病态条件下,细胞更重要的功能也许不是提高运动能力,而是积蓄一切力量,促使细胞生存。
In order to probe into the effects of endurance training on the gene expression of the aerobic respiration regulating path of diabetic GK rats, the author divided 12 rats randomly into 2 groups： a calm group （GKC, n=6） and an endurance training group （GKE, n=6）, put group GKC into treadmill training for 6 weeks, took out the gastrocnemius within 24-48h after the last time of training, tested the mRNA transcription of p53, SCO2 and COXII by means of real-time PCR, as well as the protein expression of p53, SCO2 and COXII by means of western blot, and revealed the following findings： 1） the gene transcription and protein expression levels of p53 of the rats in group GKE were significantly lower than those of the rats in group GKE; 2） comparing group GKE with group GKE, there were no signification differences in terms of gene transcription and protein expression levels; 3） comparing group KF with group GKC, there was no signification difference in terms of COXII gene transcription level, but the COXII protein expression level of the rats in group GKE was very significantly lower than that of the rats in group GKC. The findings indicate that endurance training cannot significantly boost the aerobic respiration ability of the mitochondria of diabetic rats. The significant lowering of the COXII protein expression level seems to show that the endurance training model in this experiment was harmful to their aerobic respiration axis, however, as cautiously figured by considering the result of the significantly lowering of P53 gene expression, the cause may be as follows： since the p53 gene expression level was unable to continue to maintain the normal homeostasis as affected by the course of diabetes, the lowering of its gene expression ability was extremely likely for boosting cell survival, or probably for delaying the dying or aging process of the sick cells of the GK rats. Under the condition of sickness, a more important function of cells is probably not to enhance moving ability, but to accumulate all the strengths to promote cell survival.